Fatty Liver (H&E)

Special preparations:
1. Frozen material, not paraffin
embedded
2. No alcohol dissolvant
3. Special stains: Sudan/Oil red
4. The fat is colorless so we need other
stain method to distinguish them

Alcoholism, DM,
poison
Fatty liver (Sudan)

Sudan stain
stains lipids

Fat vacuoles
cause: mushroom poisoning,
hepatitis, alcoholism

fat vacuole
Hyaline change in the kidney 989
(chronic glomerulonephritis)

Accumulation of
protein

Hyaline obliteration of
glomeruli (acellular
eosinophilic mass)

atrophy of tubule

Hyalinization: different stages of

changing on one slide

Amyloidosis: entire slide in same

stage of change.
 167
Intranuclear glycogen accumulation in the hepatocytes

Causes: DM,
genetic disorders

Vacuoles are Glycogen seen

smaller than fatty as clear space
liver with a dark
ring around

Other method for detection of

glycogen:
PAS: glycogen appears dark pink
Brown atrophy of the cardiac muscle cells 559

Lipofuscin
granules in a
cardiac myocyte

Increasing space
between cells
due to atrophy

Physiological cause: aging

Brown lipofuscin is pigment formed
through oxydation. Found near nucleus
(longitudinal section)
Pigment degeneration (endogenous
pigment degeneration)
Anthracosis of the lung

Accumulation of
charcoal
(anthracosis)

Destruction of alveolar septum.

Bigger space (emphysema)

Cause: smokers

Emphysema: destruction of alveolar

septum. Lungs are not able to
provide normal ventilation function.
Tattoo of the skin

Ink always appear near

vessels because
macrophages grab ink and
moves along vessels

vessel

ink

Hair follicle
Pathologic calcification in the kidney

Two kinds of calcification (p.41):

1. Dystrophic in area of necrosis, fine,
white granules or clumps
2. Metastatic in normal tissue because
of hypercalcemia

Calcium is
basophilic, dark
purple.

near tubules
Hydropic change (degeneration) of squamous epithelium

Features of necrosis:
1. eosinophilic
2. anucleus
3. disruption of architecture
4. inflammatory infiltrate

Vacuoles visible near

basal lamina with highest
magnification

Gangrene coagulative necrosis +

infection by bacteria (liquified by bacteria)

Fibrinoid necrosis autoimmune disease

(formed from fibrin, not fibrous connective
tissue.

vacuoles with
clear fluid

Fresh cell necrosis is eosinophilic

pink, light red
Calcified necrosis tissue is
basophilic blue
Hydropiic vacuolar degeneration
Coagulation necrosis of the cardiac muscle cells
(acute myocardial infarct)

No nuclei
Lack of architecture

Normal fibers are branched

Necrosis more pink and no

nucleus

Infiltration of
inflammatory cells into
interstitial space
Coagulative necrosis of the spleen (old splenic infarct)

3 layers:

necrosis

Fibrous capsule

Normal

hemosiderin:
early fibrous
change evidence

cholesterol ester
Caseous necrosis of the lymph node (tuberculosis)

Architecture obliterated.
Cellular outline gone.
Enclosed by inflammatory border.

lymph node
parenchyma

lymphocytes

epithelioid cells
(macrophages looking
like epithelium)

necrosis

Langerhans giant cell

(fused epithelioid cells,
many nuclei)
Enzymatic fat necrosis (acute pancreatitis)
Calcium soap

Free fatty acid + calcium > soap.

Chalky, white mass on tissue.
Stains basophilic (blue)

Destroyed fat
tissue

Calcium soap
(amorphous
basophilic deposits
between fat cells)
Liquefactive necrosis of the brain
(old cerebral infarct)

Brain looks like

fine net with
loose debris

Liquefactive necrosis most frequently

seen in the brain.
In liver, massive damage > liquefactive
Focal damage > coagulative

Necrotic debris
Liquefactive necrosis of the liver
(massive hepatic necrosis)

Massive necrosis

Causes:
Mushroom poisoning
Carbon tetrachloride exposition
(hepatotoxic)

Bile duct

Inflammatory
infiltrate
Nasal polyp (allergic)

respiratory epitheliun
(ciliated pseudostratified
columnar epithelium)

Mucoid stroma with

eosinophils

gland (maybe)

polyp stroma

Focal inflammatory swellings of mucosa of

nose or paranasal sinuses.

Remnent allergic reactions > chronic

mucosal edema & enlargement of turbinates.

Localized bulgings of the mucosa & form

polyps.

Respiratory epithelium, mucous glands within

a loose mucoid stroma.

Plasma cells, lymphocytes, eosinophils.

Thickening of basement membrane & goblet

cell hyperplasia.

lymphocyte

eosinophils (purple
nucleus, pink cytoplasm,
looks like eye)

loose, pale, connective

tissue due to edema
(caused by
inflammation)
 air bubble (water
Pulmonary edema lost during
preparation)

congested
capillary

alveoli filled with eosinophilic,

cell free fluid (transudate)

Lighter pink may be caused by

low protein content

thickened
alveolar wall
caused by dilated
capillaries and
intersitital edema

The most common cause of pulmonary

edema relate to hemodynamic alteration
in the heart that increase the perfusion
pressures in the pulmonary capillaries
and block effective lymphatic drainage:
Left ventricular failure, mitral stenosis,
mitral insufficiency
ARDS (acute respiratory distress
syndrome)
inhalation of toxic gases
aspiration of gastric contents
viral infections
uremia

Interstitial edema (asymptomatic)

> alveolar edema (short of breath)

dark purple is
macrophage?
 Acute congestion of the kidney

everything covered
with red blood cells

enlarged capillary
with RBCs

glomerulus

congestion

congested
capillary

tubule
tubules

The venous system is filled with

erythrocytes (pink cells), if with
long standing congestion we
may observe the degenerative
changes of cell in the affected
organ.

Erythrocytes in
capillaries
Chronic congestion of the liver Central vein surrounded by
hypererythmic region then by
normal hepatocytes.

Normal
hepatocytes

lighter area because of

hepatocyte atrophy

hypererythmic region
(hemorrhage necrosis).

Dense because of congestion

central vein (wall
not visible?)

Sometimes can
find portal triad

Erythrocytes

fatty change
(steatosis)

The hepatocytes in the central region of the

lobule become atrophic and with fatty
change.

Intermediate zone of the lobules filled with

erythrocytes.

Unaffected area (periportal zone) is

characteristic for chronic congestion of liver.
Purpura of the brain

Ball hemorrhage spherical lesion

composed of compactly arranged,
extravasated erythrocytes, in the center
there is a necrotic small vessel wall.

Ring hemorrhage in the center

there is a vessel plugged with
erythrocytes. The vessel is
surrounded by a ring of necrotic
brain tissue. The outer mantle
consists of a ring of erythrocytes.
 Dissecting hematoma of the aorta
outter surface
(tunica adventitia)

channel inside aorta wall

(previously filled with blood)
(wall dissected by blood)

Destroyed fibers in
tunica media with
inflammatory cells

aorta wall Aorta:

Outter surface fat
Inner endothelium

inner surface
Abnormal vessel
wall. More loose,
causes the vessel
wall dissection.
Red thrombus

Fibrin (acellular)

Cellular part of
thrombus (RBCs)

Fibrin

RBC and WBC

Eosinophilic
granulocytes
Organization and recanalization of the thrombus

Vessel wall

Capillaries in
granulation tissue
Granulation
tissue (in vessel
lumen)
Vessel lumen

Granulation tissue: specialized vascular

connective tissue involved in healing by
fibrosis (scar formation). Replaces
thrombus.

Thrombus not yet

replaced by
granulation tissue

capillary inside
granulation tissue
Disseminated intravascular coagulation
(DIC) (the kidney)

Enlarged capillary
filled with
erythrocyte

Inflammatory
infiltrate with
autolysis of
tubules

Thrombi
(acellular mass
inside capillary)

Afferent arteriole
thrombus (tail of
glomerulus)
(characteristics for
DIC)
 138
White infarct of the kidney

Necrotic area (no nuclei).

Nuclei of inflammatory
cells between structures

Normal part of
kidney

White infarct has

large area of
necrotic tissue

Features of Necrosis:
1) anucleus (no nuclei)
2) eosinophilic (more pink)
3) Coagulative necrosis: cell outline intact
Liquefactive necrosis: disruption of
architecture
4) inflammation

Glomerulus

Necrotic area (no

nuclei)
Old myocardial infarct (H&E)

Fibrous
connective tissue
surrounded by
normal fibers

Normal muscle
fiber (sometimes
with hypertrophy)
with small nuclei

Hypertrophic
cardiac muscle
cell (nucleus
larger and more
irregular)

Normal cell
(nucleus smaller
and more oval)
Old myocardial infarct (van Gieson)

Van Gieson stain:

Connective tissue red
Cytoplasm yellow
Nuclei brown/black

Cardiac muscle
cell

Fibrous
connective tissue
Hemorrhagic infarct of the lung
Erythrocytes
inside alveolar
lumen
(necrotic area)

Pseudocapsule
(barrier)

Normal lung

Fibrin VS. Fibrous tissue

Fibrin—produced in liver; a kind of protein
found in blood
Fibrous tissue—produces collagen; stained
with Van Gieson (red)

3 different slides about kidney

Congestion of kidney—everything filled with
RBC
DIC—see thrombus in glomerulli specifically
White infarct—infection area will be necrotic;

Fibrous
connective tissue

Surrounded by
fragments of
normal lung
(darker area)

Thrombus within
blood vessels

Alveolus filled
with rbc

Necrotic walls of
alveoli
A lot of
macrophages
(brown) in
Hemosiderin?! in
normal part
 Fibrinous pericarditis (257)

Eosinophilic meshwork of
fibrin exudate overlies the
pericardial surface

Pericardium
(Epicardial) layer
sometimes associated
Myocardium looks normal with fatty tissue

Fibrinous and Serofibrinous Pericarditis are

the most common kinds of pericarditis.
Lobar pneumonia (stage of gray hepatization) (202)

Alveolar lumens with

neutrophils and
macrophages

Congested capillaries

Thickened
alveolar walls

Fibrin mesh

Macroscopically, lung looks firm,

airless, liver-like (hepatization)
Purulent meningitis (203)

Subarachnoid space
filled with neutrophils
and fibrin
(inflammatory exudate)

Congested
blood vessels

Brain tissue
 Acute phlegmonous appendicitis (504)
Inflammatory
infiltrate in the
entire wall

Dense
Lumen inflammatory
infiltrate

Germinal center
(similar to those in
lymph nodes)

Sometimes can find fibrin

deposite on outter surface
(peritoneal surface) of appendix.
Not visible in these two pictures.
Lung abscess (304)
Lung tissue
(normal part)

neutrophils

Neutrophils
with necrotic
debris. Pus

Chronic abscesses are surrounded by

fibrous wall.
Acute proliferative (poststreptococcal) glomerulonephritis (359)

Reduced Bowman space

Increased cellularity in glomeruli.

Hypercellularity is due to
intracapillary leukocytes
(neutrophils and monocytes) and
proliferation of glomerular cells.
Condyloma acuminatum (208)
Condyloma acuminatum is a benign
sexually transmitted tumor caused by
human papillomavirus (HPV, usually
type 6 or 11)

irregular outline
with columnar
epithelium

Koilocytosis: Cytoplasmic
vacuolization of the squamous
cells (characteristic of HPV
infection).
Halo around nucleus

Condylomata acuminata occur

on any moist mucocutaneous
surface of the external genitals
Macronodular cirrhosis (H&E) (206)
HBV, HCV
submassive
confluent

nodules of hepatocytes
surrounded by fibrous
connective tissue

inflammatory
infiltrate

Initially the developing fibrous

septa extend through sinusoids
from central to portal regions as
well as from portal tract to portal
tract.
Laennec cirrhosis: Ischemic
necrosis and fibrous obliteration
of nodules. Tough, pale scar
tissue
Macronodular cirrhosis (van Gieson) (207)

fibers stain pink

submassive
confluent

inflammatory
infiltrate

hepatocytes
yellow/green
 Miliary tuberculosis of the lung (210)

Macro: yellow
nodular lesions

caseous necrosis.
granulomas

Langhan's giant cell.

(Fusion of epithelioid cells.
Nuclei on the edge.)

lymphocytes

epithelioid cells
surrounds
caseous necrosis

Miliary pulmonary disease

Mycobacteria drains through lymph → right atrium → pulmonary arteries
Miliary lesions can be scattered throughout lung. They can coalesce and
consolidate lobes of lung.

If the tuberculosis organism goes through pulmonary vein to the heart,

hematogenous dissemination to every organ.
● Miliary tuberculosis most prominent in liver, bone marrow, spleen,

adrenals, meninges, kidneys, fallopian tubes, epididymis.

Sarcoidosis of the lymph node (211)
Noncaseous (non necrotizing)
granulomas.
* No central caseous necrosis.

epithelioid
cells

Giant cell
Giant cells (different kinds):
● Langhan's giant cells, nuclei on the edge

● Foreign body giant cells, nuclei NOT on the edge

Inside giant cells can be:

● Schaumann bodies: laminated layers of calcium

and proteins
● Asteroid bodies: stellate inclusions

lymphocytes

Sarcoidosis:
noncaseous granulomas + epithelioid cells + giant cells + lymphocytes.
* Lymph nodes involved in almost all cases
Luetic (syphilitic) mesaortitis (212)

In the wall or aorta, syphilis

causes syphilitic aortitis and
mesoaortitis

elastic
fibers

Perivascular
lymphoplasmacytic
infiltrate:
small vessels
infiltrate around small vessels

lymphocytes +
plasma cells in
infiltrate

Stages of syphilis
Primary: chancre
Secondary: palmar rash. Lymphadenopathy. Condyloma latum.
Tertiary: Neurosyphilis. Aortitis. Gummas
Cytomegalic inclusion disease (the kidney) (658)
Enlarged duct

Normal duct

Intranuclear basophilic
inclusion surrounded by
clear halo (Owl's eye)

● Cytomegalovirus causes enlargement

of infected cells
● Particles of virus in cytoplasm,
forming small granules and a
massive inclusion body (owl’s eye)
● Usually infect ducts. (glomeruli may
appear normal). Massively enlarged
duct, with enlarged cells lining the
lumen.

● Disseminated CMV (life threatening)

● Lungs (pneumonitis

● GI tract (colitis)

● Retina (retinitis)

● Congenital infections cause

cytomegalic inclusion disease (CID)
● Mental retardation

● Hearing loss

● Neurologic impairments
 Rhinoscleroma (the nasal cavity) (213)

Mikulicz cells – foamy macrophages

● Macrophages with clear abundant
cytoplasm and small, dark nucleus

Chronic granulomatous infection caused by Klebsiella rhinoscleromatis

● Gram-negative, encapsulated, nonmotile, rod-shaped bacillus (diplobacillus), member of the
Enterobacteriaceae family

3 main stages
1) Catarrhal/atrophic: rhinitis → rhinorrhea
2) Granulomatous: bluish red nasal mucosa. Polyps. Destruction of nasal cartilage (Hebra nose)
3) Fibrotic stage: sclerosis and fibrosis

Cornill’s cells – plasmocytes with hyalinized IgG antibodies inside the cytoplasm (hard to find)

Russel’s bodies – deposits of hyalinized IgG outside the cells (very hard to find)

Stains for bacteria: PAS, Giemsa, Gram, and silver staining

Plenty of inflammatory cells with small empty spaces (Mikulicz cells)

Actinomycosis (the oral cavity) (217)
Appearance
● GRAM + hyphae, neutrophils,
macrophages with lipids and
sometimes companion bacteria: rods
and cocci
● Foamy macrophages (not Mikulicz
cells, the name is reserved for
rhinoscleroma)
● Amorphous dark purple area is the
colony, surrounded by neutrophils

colony of Actinomycetes
● bacteria with long
branching filaments

surrounded by
neutrophils

Abdominal is the most common infection

Facial infection caused by infected root canal (usually secondary infection)

Actinomyces israelii
● bacteria with long branching filaments. Gram-positive
● anaerobe, normal flora of mouth
● may invade after trauma like broken jaw or dental extraction
● Sulfur granules
● not communicable
Candidiasis (the esophagus) (H&E; PAS) (218)

yeast (single cell) and

hyphae or pseudohyphae

Candida albicans
● Normal flora of skin and mucus
membrane
● Oval yeast with single bud.
Pseudohyphae is infectious form.
● Can appear as yeast,
pseudohyphae, true hyphae (less
common in tissue)
● Thrush, vaginitis, diaper rash

Trush: superficial infection, usually in oral cavity

Invasivce candidiasis in immunocompromised patients

Microabscesses: candida in yeast and pseudohyphae form + neutrophils

Pseudohyphae: budding yeast cells joint together into a string

Aspergillosis (the lung) (219)
Aspergillus (a kind of mold)
● Healthy people: allergies (brewer's
lung)
● Immunocompromised: sinusitis,
pneumonia, fungemia
● V-shaped branching with septate
hyphae.
● High IgE

Invasive aspergillosis:
●

● Disseminated aspergillosis only in

immunocompromised patients

●Fungus ball in lung can be seen in non

immunocompromised people.
● There is a gap between tissue and
fungal ball.
● Usually grows in preexisting
cavities (caused by tuberculosis or
abscess)
● Sparse inflammation. Chronic
inflammation may cause fibrosis
● Does not invade other tissues

Trichosis
●

tennis racket shape (shorter

stalks than candida)
Cryptococcosis (the lung) (mucicarmine) (320)
Stainings
● India-ink staining: visualization
of the mucous capsule
● Mucicarmin - the mucous
capsule is red
● PAS - cryptocccus as pale,
round object
● Hotchi method: PAS + Giemsa
+ Alcian blue

Mucicarmin stains cryptococcus

mucous capsule pink.
Only yeast, no Small red/purple circles
pseudohyphae or hyphae
H&E is not specific for
cryptococcus

Cryptococcus neoformans
● Widely in nature, especially soil with pigeon droppings.
● No human to human transmission.
● Yeast. Seen in CSF with India ink. Large unstained capsule.
● Disseminated disease in immunocompromised
● Most common life-threatening fungal disease in AIDS
patients. Disseminates to CNS and other organs.
 Trichinellosis (the skeletal muscle) (222)
inflammatory cells.
Eosinophils respond
to parasites

Trichinella larva.
● Can live for years before dying

and calcifying
● Usually asymptomatic

nurse cell (paler)

Muscle cells

parasites
● If in right atrium, can be fatal
(arrhythmia, SA node)
● In children, usually causes abdominal
pain instead of malnutrition. Can check
for eosinophilia, although it's nonspecific.
Trichinella spiralis
● Nematode
● Undercooked pig meat
● Larvae grow and multiply in the gut
● Hematogenous dissemination, penetrate muscle cells
● Fever, myalgias, eosinophilia, periorbital edema
Schistosomiasis (the urinary bladder) (224)

Egg (calcified)

Granuloma. Chronic
granulomatosis inflammation
surrounded by fibrosis

fibrosis

Foreign body giant cell

(nuclei not on the edge)

Non-calcified egg

In liver, blocks bile ducts, leads to

cholestasis, destruction of liver, liver
failure. Protein loss, hydroperitoneum

Schistosoma mansoni and japonicum

● Liver

● Mortality from hepatic

granulomas and fibrosis

● Can spread to lung and spleen

Schistosoma haematobium
● Bladder

● Hematuria and granulomatous

disease of bladder
● Chronic obstructive uropathy
Lupus nephritis (357)
Wire loops
thickening of
capillary (wire loop)
SLE is a systemic autoimmune disease
● Women 20-40
● Antibodies against DNA, nuclear proteins
● Kidney, joints, serous membranes, skin
Injuries due to
● Deposition of immune complex
● Antiphospholipid antibodies causing
thrombosis of capillaries
Diagnosis
● 1-Smith antigen – soluble nuclear antigen
complex
● 2- antibody to double-stranded DNA
Immune complex-mediated glomerulonephritis
Diffuse or focal
proliferation of
mesangial cells in
glomeruli
Characteristics:
● Narrow lumen of capillaries in
glomeruli
● Proliferation of cells; hypercellular
pattern
● Delicate, homogenous thickening of
capillaries
● Wire-loop lesion
● Subendothelial deposits (between
endothelium and basement
membrane) of immune complexes
● Thickened, hyalinized loops of
capillaries
● Usually in Class IV (also in III and
V)
● Indicates active disease
5 patterns of SLE glomerular injury:
Class I: minimal or none (rare)
Class II: mesangial lupus glomerulonephritis
● Mesangial proliferation
● mesangial matrix, deposits of IgG, IgM, IgE
and Complement
Class III: focal proliferative glomerulonephritis
● Only portions of each glomerulus affected
Class IV: diffuse proliferative glomerulonephritis
● Proliferation of endothelial, mesangial,
sometimes epithelial cells
● Most serious. All glomeruli affected
Class V: membranous glomerulonephritis
● Widespread thickening of capillary walls
 Rheumatoid nodule (the skin) (215)

Subcutaneous rheumatoid nodule with

1) Large area of fibrinoid necrosis,
surrounded by palisade of
2) Macrophages and inflammatory cells

Rheumatoid nodule
● Arise in skin subjected to pressure

○ Elbow, knees

○ Movable, rim, rubbery, large, may

ulcerate
● Central core of fibrinoid necrosis

○ Fibrin and other proteins (degraded

collagen)
● Rim of macrophages – palisading pattern

● Peripheral to the macrophages –

lymphocytes, plasma cells

Systemic, chronic inflammatory disease

Women 30-50 years

Rheumatic arthritis
● Involves joints symmetrically and bilaterally

● Small joints first – hand, wrist, elbows, ankles

RF (rheumatic factor) – Antibodies against the Fc fragment of IgG

● 80% of cases, multiple antibodies, IgM, sometimes IgG or IgA detected
 Scleroderma (the skin) (851)

very thin atrophic

epidermis

In dermis, no appendages
(hair follicles)

SS (systemic scleroderma) – vasculopathy,

excessive collagen deposition in the skin and
other organs – lungs, GI, heart, kidney
● Thinning epidermis
● Loss of rete pegs
● Atrophy of dermal appendages
● Obliteration of capillaries
Rete pegs - epithelial ● Deposition of collagen
Normal skin extensions that project ● Few inflammatory cells - lymphocytes
into the underlying
epithelium connective tissue CREST syndrome
● C-calcinosis
● R-Raynaud phenomenon
● E-esophageal dysmotility
● S-sclerodactyly
● T-telangiectasia

Lamina propria (underlying connective tissue)

Polymyositis (216)

fragmented muscle
fibers

inflammatory
infiltrates

Polymyositis
● Chronic inflammatory myopathy

● Dermatomyositis: when skin is also

involved

Higher risk:
● Women, blacks

● Patients with malignancy

(paraneoplastic syndrome)

Signs
● Weakness of muscle

● Destruction of the skeletal muscles

by cytotoxic T cells
● Dermatomyositis – rash on the

upper eye lids, face, trunk

● Infiltration of the inflammatory

cells mostly within the fascicles

● Focal necrosis

● Fibrosis

● Regeneration of the single muscle

fibers. Enlarged nuclei and

basophilic cytoplasm
Polyarteritis nodosa (the heart) (H&E) (268)
fresh fibrinoid necrosis

obliterated
lumen

Vessel surrounded by
adipose tissue

Stages:
1.Deposit of immune complexes (in small
and medium arteries)
2.Inflammation (transmural inflammation
of the arterial wall)
3.Fibrinoid necrosis in vessel wall
4.Fibrosis
All stages may coexist in the same vessel

inflammatory Acute necrotizing vasculitis of small or medium-sized

infiltrate muscular arteries
○ Typically renal and visceral

○ Ischemia and infarction of affected tissue

○ Symptoms depends on the affected organ (the most

common – kidney, heart, skin, skeletal muscle,

mesentery)

● Women
● Fatal without treatment
● Lesions may involve entire circumference of the vessel
wall or part of it
● Central fibrinoid necrosis
● Acute inflammatory response, fibrosis
● Thrombosis in affected arteries, infarcts, aneurysms
● Azan staining – fibrinoid necrosis – red
Polyarteritis nodosa (the heart) (azan) (269)
In azan staining, fibrinoid is red

fresh fibrinoid necrosis

adipose tissue
Hashimoto thyroiditis (459)

colloid in
follicle

destruction of gland
by inflammatory
infiltrates

germinal
center

● Struma lymphomatosa, lymphadenoid

goiter
● Most common cause of goitrous
hypothyroidism in regions that have a
sufficiency of iodine
● Women, 40-50, rare in children
● Organ – specific autoimmune disease
● The increased risk of lymphoma and
carcinoma
● Symptoms related with hypothyroidism
● Diffuse, asymmetric enlargement of the
gland

Microscopically:
● Chronic inflammatory infiltration –

lymphocytes
● Presence of lymphoid follicles with

germinal centers
● Oxyphilic metaplasia – Hurthle cells

(cells with eosinophilic cytoplasm)

● Atrophy of thyroid follicles

● Interstitial fibrosis
Amyloidosis (the kidney) (H&E) (362)

Amyloid in glomerulus
(homogenous mass).
Glomerular architecture
obliterated by amyloid.

Amyloid
Group of diverse
extravascular/extracellular protein
deposits that have:
1. Common morphological properties
2. Affinities for specific dyes
3. Characteristic appearance under
polarized light

● Amyloidosis can be primary, or

secondary to malignancies, chronic
inflammatory diseases, or drug abuse
● Most common affected organs – kidney,
heart, liver, GI
○ Affected organs generally:
Kidney ■ Enlarged (but function is low)
● Deposition of amyloid – pink
■ Firm
around area ■ Waxy appearance
● All glomeruli involved

○ Enlargement of glomeruli
● Amyloid – fibrillogenic protein
● Hypocellularity

● Capillary obliterated
Staining
● Congo red stain amyloid red

● Thioflavin T – fluorescence assay for

amyloid
Amyloidosis (the kidney) (Congo red) (374)

amyloid

Polarizing
microscopy gives
the orange masses
greenish tinge

Glomerulus
filled with
amyloid
Granulation tissue (101)

Loose ECM with inflammatory cells

Capillary filled with RBC

Granulation tissue
● Contains small blood vessels
(endothelial cells) (angiogenesis)
and fibroblasts
● Organization (necrosis, thrombus)
● Tissue repair - scar
Foreign body granuloma (102)

Crystals? (foreign bodies)

Giant cell (macrophage)

Epithelioid cells

Foreign body granulomas

● Caused by inert foreign bodies which do
not cause inflammation
● Surrounded by epithelioid cells,
multinucleated foreign body giant cells,
various inflammatory cells and connective
tissue.
Simple endometrial hyperplasia (103)

Lumen is dilated,
looks like cystic gland

Increased number
of cells

“Simple” - lower grade hyperplasia

“Atypical” - higher grade

Hyperplasia - an increase in the

number of cells in an organ or
tissue usually resulting in
increased volume of tissue.

Simple endometrial hyperplasia

● Gland of various size and shape, with cystic
glandular dilations
● Associated with prolonged estrogen stimulation
● Increased proliferation of glands
● Increased gland-to-stroma ratio
● Higher risk of carcinoma
 Myocardial hypertrophy (275)

Enlarged nuclei

Fibrosis (scar)

Myocardial hypertrophy
● Cells increase in size and have enlarged
hyperchromatic nuclei
○ Cardiac myocyte can't divide, so
hyperplasia can't occur
● Physiologic and pathologic
● Chronic hemodynamic overload
(hypertension, valvular diseases)
 Testicular atrophy (560)

Spermatic tubules

Loose interstitial tissue

Arrest in the development of

germ cells (no spermatogenesis)

Sertoli cell

thickened basement
membrane with
hyalinization

Testicular atrophy
● Decreased size of cells
○ decreased size of organ
● decreased workload
● loss of innervation
● diminished blood supply
● inadequate nutrition
● loss of endocrine stimulation
● aging
● pressure

Cryptorchidism
● Hypopituitarism
● Malnutrition
● Irradiation
● Administration of estrogens
Myositis ossificans (104)

Myositis ossificans - bone

formation in the muscle as a
result of injury.

eosinophilic
muscle fiber

fibrosis

bony trabecula

Eosinophilic muscle fibers

● Metaplasia - reversible change of one

adult cell type (epithelial or mesenchymal)
replaced by another adult cell type
○ Adaptive mechanism

● Connective tissue metaplasia is the

formation of cartilage, bone, or adipose
tissue (mesenchymal tissues) in tissues
that normally do not contain these
elements
● May be a result of injury
Intestinal metaplasia (chronic active gastritis) (PAS & alcian blue) (144)

Gastric glands

PAS stains
intestinal goblet
cells blue (shouldn't
be in stomach)

Goblet cells admixed

with gastric foveolar epithelium.

Intestinal metaplasia
● Epithelial metaplasia -
epithelium in the stomach is
replaced by intestinal type.
● Chronic reflux of duodenal
contents
Cervical intraepithelial neoplasia (CIN II) (moderate dysplasia of the
squamous epithelium) (106)

● Disorganized squamous epithelium with

Koilocytic atypia enlarged nuclei
● Hyperchromatic
● CIN1: 1/3 thickness of epithelium
composed of changed cells.
● CIN2: 2/3
● CIN3: Full thickness of epithelium
CIN II
● An alteration in the size, shape, and organization of the
cellular components of a tissue
● Not the whole thickness of epithelium contains nuclei
● Screen with pap smear

Cellular dysplasia (true dysplasia)

● Abnormal development of cells
Histological dysplasia (fibrocystic dysplasia of the breast)
● Macroscopic abnormal development of tissue

Cervical intraepithelial neoplasia (CIN) classification:

● CIN I, mild dysplasia
● CIN II, moderate dysplasia
● CIN III, severe dysplasia

● CIN I is low-grade squamous Intraepithelial Lesion (SIL),

CIN II and III are high-grade.
○ CIN II and III are not reversible.
Cervical intraepithelial neoplasia (CIN III)
(preinvasive squamous cell carcinoma/in situ carcinoma) (108)

Nuclei in full thickness of

epithelium (Dysplasia).
Lack of maturation of the
epithelium (anaplasia).

No invasion

CIN III
atypia ● In situ carcinoma - doesn't
penetrate basement membrane
● Epithelium shows altered
architecture and abnormalities in
cytology and differentiation
● Stage 0 cervical cancer

Carcinoma
● Malignant epithelial cancer
● Lesions are white with sharp
margin

Histopathology:
● anaplasia, atypia, mitotic figures
may be numerous
● neoplasm don't cross basement
membrane
● Partial replacement of
endocervical glandular epithelium
by CIN III.
Invasive squamous cell carcinoma of the uterine cervix (109)

Crosses basement
membrane (invasion)

Nests of malignant
squamous epithelium.
Neoplastic cells in deeper
layers (not only in the
epithelium)

Mass of neoplastic
cells with central
keratinization

Keratin pearls: concentric

keratin circles
Invasive squamous cell carcinoma
● Most common cervical cancer (80%)
● Precursor is high-grade squamous intraepithelial lesion (HSIL) (CIN II and III)
● Can be fungating (exophytic) or infiltrative cancer (endophytic)
○ Fungating: breaks on the skin or surface of an organ
▲ Papillary or polypoid excrescence on the surface
○ Infiltrative: invades surrounding tissue
▲ Infiltrates bladder, wall of large bowel, wall of vagina
● Could be caused by HPVs
● Peak incidence 45 years old
Tubulo-villous adenoma of the colon (117)

Tubulovillous adenoma
composed of
● tubular and
● villous
structures, each comprising
>20% of tumor

Categories of adenoma
● Tubular: pedunculated polyps.
Small rounded (tubular) glands
● Villous: often sessile.
Slender villi
● Tubulovillous: mixed

Nuclear hyperchromasia,
elongation, and stratification.

Tubulo-villous adenoma of the colon

● Benign neoplasm of the glandular epithelium origin. Encapsulated.
● Precursors to colorectal cancer
● Can evolve to adenocarcinoma (especially when it contains dysplastic
epithelium) - cancer of the colon arises in adenomatous polyps
● Neoplastic epithelium cover fibro-vascular core
● The pedicle is covered by normal intestinal mucosa
● Characterized by epithelial dysplasia
○ Crowded nuclei. (1 layer of cells in normal tissue)
● Can be pedunculated or sessile
○ Usually pedunculated with fibromuscular stalk.

When analyzing colonic polyp for malignancy, need to check entire polyp to
see if it's benign.
Look for pedicle to make sure the whole structure is taken.
Mucinous adenocarcinoma of the colon (H&E) (11)

Mucinous lakes
● Massive production of mucinous
material.
○ Too much mucin destroys
glands.
● There is another type which
produce mucus inside cells (no
mucus lake)

Small, dark cells with lack of

cytoplasm (mostly nucleus) are
neoplastic. Secretes lots of
mucus surrounding the cell.

Mucinous adenocarcinoma
● Malignant epithelial neoplasm arising from the glandular mucosa
● Contains extracellular mucin comprising more than 50% of the tumor
● Mucinous deposits are interspersed with small nests of carcinoma cells with
cytological features of malignancy (hyperchromasia of nuclei, pleomorphism,
enlarged nuclei with nucleoli, abundant mitoses - sometimes atypical)

Macroscopically:
● Polypoid
● Ulcerating
● Infiltrative
Macrofocal infiltration of the breast cancer (116)

Infiltration is typical feature

of malignancy (local invasion
with destruction of the
surrounding tissues)

Fibrous stroma

Nests of neoplastic cells on the

border of the tumor

Neoplastic cells with enlarged,

hyperchromatic nuclei, scant
cytoplasm, distinct nucleoli
● polymorphism
● greater mitotic activity

● >95% of breast
malignancies are
adenocarcinomas
● Breast cancer genes:
BRCA1 and BRCA2
Forms of infiltration (cancers):
● macrofocal: large nests of neoplastic cells
● microfocal
● dispersed

Metastasis
● Tumors implants discontinuous with the primary tumor
● Pathways of spread:
○ direct seeding of body cavities or surfaces
○ lymphatic spread
○ hematogenous
○ cerebrospinal fluid

Cytological features of malignant neoplastic cells:

● Large, hyperchromatic, large nuclei with weird shape
Neoplastic cells in peritoneal fluid (adenocarcinoma of the colon) (140)

Malignant tumor, epithelial origin

Neoplastic cells floating in

peritoneal fluid

mucin

Serous fluid in peritoneal space?

● Direct seeding of natural body cavities: peritoneal, pleural,

pericardial, subarachnoid, joint space
● Cytologic examination
● Neoplastic cells with cytological features of malignancy
Pulmonary neoplastic embolism (adenocarcinoma of the colon) (114)

Nests of neoplastic
cells next to vessel

vessel

Signet ring cell carcinoma:

clear vacuole, nucleus
squeezed to the side

● Lymphogenous spread is typical

for carcinomas
● Hematogenous spread typical for
sarcomas
● Lymphatic vessels are filling with
neoplastic cells with
hyperchromatic nuclei
● The most frequent localization of
hematogenous metastases are
liver and lungs
● Neoplastic cells invade tissues,
destroy blood and lymphatic
vessel walls
Metastatic carcinoma in the lymph node (esophageal squamous cell
carcinoma) (139)

Germinal center Fibrous capsule

Neoplastic cells

Keratin pearl

Histopathology:
● focal nodal involvement
(especially in early stage)
● definite nesting
● sometimes extensive necrosis
● keratinization
● intercellular bridges

● Lymphatic drainage is the most common

pathway for the dissemination of carcinomas
● The pattern of lymph node involvement follows
the natural routes of lymphatic drainage

Macroscopy:
● Lymph node with metastasis is larger or
normal in size (it depends on amount of
neoplastic cells)
● Nodal metastases of squamous cell carcinoma
have particular tendency for cystic change
Metastatic carcinoma in the ovary (gastric signet ring cell carcinoma)
(Krukenberg's tumor) (611)
Krukenberg’s tumour
● Metastatic mucinous/signet ring
cell adenocarcinoma of the
ovaries which typically originates
from primary tumors of the GI
tract, most often stomach.
● Usually >40 years of age

Macroscopy:
● Usually bilateral tumors
● Moderate solid multinodular
enlargement of the ovaries

Histopathology:
● diffuse infiltration by signet ring
cells (containing abundant
mucin with depressed nucleus
on the border of cell)
● highly fibrous stroma
(desmoplasia)

Signet ring cells

● Neoplastic cells with mucus
(clear area) inside with nucleus
on the edge
● Mucicarmine stains mucin red
Leiomyoma of the uterine corpus (129)

Leiomyoma
● Benign, well-differentiated
○ Malignant transformation rare
● Usually in myometrium of uterine
corpus
● The most common tumor of the
female genital tract
● Develops usually in reproductive
age
● Interlacing bundles of neoplastic
smooth muscle cells
○ Identical to normal smooth
muscle cells in the
myometrium.
● Usually asymptomatic
○ Dysmenorrhea, pain,
compression, sometimes
infertility

Macroscopy:
● Solid, firm, pale gray, well
circumscribed tumor without
encapsulation
● Round to oval in shape
● It range in size from 1 mm to
over 30 cm
● Intramural, subsearousal,
submucosal
● Singular lesion or multiple
tumors

Whorled bundles of normal

looking smooth muscle cells
Leiomyosarcoma of the uterine corpus (130)

Leiomyosarcoma
● Malignant tumor composed of
cells showing distinct smooth
muscle features
● Usually in uterus, intestine,
stomach
● Develop de novo from the
myometrium or endometrial
stroma

Macroscopy:
● Singular soft tumor
● Pink-gray-yelowish in color
● Bulky, fleshy tumor that invade
the uterine wall or polypoid mass
that project into the uterus cavity
● More than 5 cm

Histopathology
● Spindle cells showing distinct
smooth muscle features
● High mitotic activity
● Wide range of atypia
● Well differentiated to
anaplastic
● Zonal necrosis and hemorrhage

Wide range of atypia

Some smooth muscle features
 Lipoma of the skin (121)
Conventional lipoma (most
common type):
● Well encapsulated (fibrous
capsule)
● Mature adipocytes that varies
in size. Identical to surround
adipose tissue
● Distinct cell borders, round
nuclei situated at the periphery
and optically empty cytoplasm
● No pleomorphism

Fibrous capsule?
Skin (dermis and epidermis)

Normal looking adipose tissue

Lipoma
● Benign tumors of mature adipocytes
● The most common soft tissue mesenchymal neoplasm in adults
● Occurs in any age, but most common between the ages of 40 and 60 years
● More frequent in obese individuals
● 5% of patients have multiple lipomas

● Localization:
● Within subcutaneous tissue (superficial lipoma)
● Within deep soft tissues (deep lipoma) as intermuscular or intramuscular lipoma
● On the surfaces of bone (parosteal lipoma)

Macroscopy:
● Well circumscribed, lobulated tumor
● Yellow, greasy cut surface
Myxoid liposarcoma (the skin) (122)
Liposarcoma
● Malignant tumor. Mesenchymal
cells and lipoblasts in a
prominent myxoid stroma
● A peak incidence in the 4th and
5th decades of life

Localization
● Deep soft tissues of the
extremities (the musculature of
the thigh), rarely arises primarily
in the retroperitoneum or
subcutaneous tissue
Myxoid?
● Tendency to recur locally
● One-third of patients develop
distant metastases in unusual
soft tissue (retroperitoneum,
opposite extremity, axilla) or
bone (spine), later spread to
lung

Lipoblasts: primitive cells with

small lipid vacuoles

Histopathology:
● Uniform round to oval shaped primitive nonlipogenic
mesenchymal cells
● Small signet-ring lipoblasts
● A prominent myxoid stroma rich in a delicate capillary
vasculature

Macroscopy:
● Well-circumscribed, multinodular tumor, showing a tan,
gelatinous cut surface
Pleomorphic rhabdomyosarcoma (soft tissue of the neck) (131)

Pleomorphic rhabdomyosarcoma
● Malignant
● Polygonal, round, and spindle cells
with evidence of skeletal muscle
differentiation
● occurs almost exclusively in adults,
is more common in men and
present at a median age in the 6th
decade

Localization:
● Deep soft tissues of the lower
extremities

Macroscopy:
● Well circumscribed, usually large
tumors (5-15 cm), often surrounded
by a pseudocapsule
● The cut surface is whitish and firm
with haemorrhages and necrosis

Histopathology:
● Composed of undifferentiated
round, spindle, and polygonal cells
with densely eosinophilic cytoplasm
in spindle, tadpole, and racquet-like
contours - rhabdomyoblasts.

Numerous large, sometimes

multinucleated bizarre
eosinophilic tumor cells

Racquet or tadpole shaped

Desmoid (126)

Normal cells trapped by fibers

Fibrous tissue

● Clonal fibroblastic proliferations

that arise in the deep soft tissues
and are characterized by
infiltrative growth and a tendency
toward local recurrence but an
inability to metastasize
● = Deep seated fibromatosis
● = Desmoid-type fibromatosis

Localization:
● Extraabdominal (shoulder, chest
wall, back, thigh, head and neck)
● Abdominal (tumors arise from
musculoaponeurotic structures of
the anterior abdominal wall)
● Intraabdominal (pelvis and
mesentery)

Macroscopy:
● Firm lesion
● The cut surface reveals a
glistening white, coarsely
trabeculated surface, resembling
scar tissue
● 5-10 cm in diameter

Histopathology:
● Poorly circumscribed lesion with
infiltration of the surrounding soft
tissue structures
● Elongated, spindle-shaped cells of
uniform appearance with small,
pale-staning nuclei and 1 to 3
nucleoli
● A collagenous stroma containing
vessels
Cavernous hemangioma of the liver (133)

● Benign vascular neoplasm with

formation of large, dilated
vascular channels
● The most frequent benign
tumor of the liver
● More frequent in females
● Occurs at all ages but is least
common in the pediatric age
group
● Only large symptomatic tumors
require surgical excision

Macroscopy:
● Vary from a few millimeters to
huge tumors („giant”
hemangiomas) that can
replace most of the liver
● Usually single and soft, well
circumscribed
● When sectioned they partially
collapse due to the escape of
blood and have a spongy
appearance

Histopathology:
● Composed of blood-filled
vascular channels of varied
size, lined by a single layer of
flat endothelial cells supported
by fibrous tissue
● Thrombi may be present
● Older lesions show dense
fibrosis and calcifications
Malignant melanoma of the eyeball (136)

● Malignant neoplasm derived from

melanocytes
● Most frequently localized in the
skin
● Ocular localization: from the uvea
(iris, ciliary body and chorioid)
● The most common primary
malignant tumor of the eyeball in
whites
● Can develop as primary tumor or
in the nevi
● Hematogenous distant
metastases (most common in
liver)

Macroscopy:
● Can grow into the eyeball or
sometimes into the cranial cavity
as solid, irregular pigmented
tumor

Histopathology:
● Callender classification
○ Spindle A melanomas
○ Spindle B melanomas
○ Epithelioid melanomas
● Mixed cell type melanomas
● Necrotic melanoma
● Staging (in the skin): Clark and
Breslow scales

Epithelioid melanomas
(resembles epithelial cells)
(malignant)
 Mature teratoma of the ovary (137)
Fibrous tissue
● One of the germ cell tumors
● Composed of tissues
representing different germinal
layers (endoderm, mesoderm
and ectoderm)
● Bilateral in 10 to 15% of cases
● Composed exclusively of well
differentiated, mature tissues
(when it have immature, fetal-
like tissues: immature
teratoma)
● In children (in the 1st and 2nd
epithelium sebaceous gland year of life) and in young
adults

Macroscopy:
● Most benign teratomas are
cystic and called „dermoid
cysts”
● Unilocular, cystic tumor
containing hair and sebaceous
material
● Lined by gray-white epidermis
● Nodular foci in the cyst wall
containing tissue of three
germ cell layers (mammary
bodies or Rokitansky nodules)

Sweat gland? Microscopically:

● Cyst wall composed of
adipose
stratified squamous epithelium
with underlying sebaceous
gland, hair shafts and other
skin adnexal structures
● Other completely differentiated
tissues in mammary body eg.:
smooth muscle, cartilage,
bone, teeth, respiratory tract
epithelium, brain tissue,
thyroid (struma ovarii)
 Cartilage

Fibrous tissue
Chronic congestion of the lung (brown induration) (302)

spaces filled by air (might

be filled by edematous
fluids)

Coal dust (Black irregular

spots)

alveolar walls

Heart failure cells

(Single cells containing
dark dots)

● Chronic LVF - impairment of the exit of the blood from the lungs
● Increased pressure in the alveolar capillaries
● Microhemorrhages into the alveoli, red blood cells are phagocytosed by
macrophages (heart failure cells) (macrophages laden with
hemosiderin)
● Fibrosis of the interstitial spaces of the lung
● Lung is brown and firm – brown induration
● Consequences of higher pressure in capillaries is pulmonary
hypertension, which may lead to right heart failure.
Emphysema of the lung (2)

Ruptured alveoli, forming

large airspaces (less surface
area)

Bronchus?

Pores of Kohn ● Chronic lung disease

characterized by permanent
enlargement of the airspaces
● Visible enlargement of the
airspaces.
● major cause – cigarette smoking
(protease-antiprotease theory)
● Alpha-1 antitrypsin (α1-AT)
deficiency – 1% cases
● Emphysema is classified
according to the location of the
lesions within the pulmonary
acinus:
● Centriacinar (Centrilobular)
● Panacinar (Panlobular)
● Paraseptal
● Irregular

Coal dust (smoking?)

Bronchopneumonia (303)

Bronchioles
filled with pus

Lots of rbc and neutrophils

● Caused by infection of air way (trachea, bronchi)

● Streptococci, staphylococci
● Multifocal changes
● Four stages, but we can observe different stages in every focus.
● Pneumonia has 4 stages:
● Congestion
● Red hepatization
● Gray hepatization
● Resolution
● macro: multifocal changes. Inflammations are yellow.
● Usually complication of bronchitis.
● Slide:
● Normal area: some fluid in normal area (septa visible).
● Inflamed area: Septa almost invisible (lots of cells in exudate
compresses the septa). Bronchi filled by pus (inflammation start
in bronchi, then involves other areas) (neutrophils, cellular
debris).
Interstitial pneumonia (305)

Artery?

● Wide bronchoalveolar septa

filled with inflammatory cells
● Necrotic debris on wall of
septa, forming hyaline
membranes. Serious state

No infiltration in bronchus

Enlarged capillary
in septa filled with
blood cells

Empty alveolar spaces

● The most common cause is viral infection of the lung

● CMV, Varicella, HSV
● Viruses affect the alveolar epithelium and cause mononuclear infiltration
● Children, elderly patients
● Often asymptomatic, no changes in x-ray picture
● Dilated interstitial parts of the lung, airspaces preserved
● Symptoms: cough for a long time. Reduced lung capacity.
● Necrosis of type I epithelial cells and hyaline membranes formation
● Morphology: no circumscribed changes. More yellow areas suspected (in
autopsy sample). Newborn might die from interstitial pneumonia
● slide: thickened septa containing cells (Inflammatory cells (lymphocytes,
plasma cells). Dilated capillaries. Hyaline membrane covers septa wall (from
necrotic debris of injured cells). Can cause death when large areas covered.
Bronchi normal with no infiltration.
Fibrocaseous tuberculosis of the lung (306)

Large area of necrotic debris

epithelioid cells
Langhans giant cell

Inflammatory infiltrates

● Caused by Mycobacterium tuberculosis

● Inhaled M. tuberculosis is deposited in the alveoli, usually in the
lower and middle lobes and anterior segments of upper lobes.
● Generally is transmitted from person to person by aerosolized
droplets
● Caseous granuloma - Classic lesion of tuberculosis
● Soft, semisolid core surrounded by epithelioid cells, Langhans
giant cells, lymphocytes and peripheral fibrous tissue
● Caseous necrosis in center
● This is why this form of tuberculosis is called fibrocaseous
tuberculosis

● Gross: large nodule (white, chalky appearance), caseous necrosis.

Granuloma at the edge.

● Slide: Edges of necrosis fibrosis (fibrous connective tissue surrounds

granulomas). Lesions are large (unlike in miliary tuberculosis)
 Tuberculoma (319)

Necrosis (old granuloma)

New granuloma on the edge

fibrosis

● Firm, round tumor (not neoplastic)

● Lung, meninges
● Solitary mass with central caseous necrosis surrounded by granulomatous tissue
● Encapsulated
● Can form when treating tuberculosis. If treatment stops, new granuloma forms
around healing areas (fibrotic areas).
● Up to 10 cm. Looks like malignant tumor.
● In tumor with central necrosis, need to check border to determine cell type to
differentiate form neoplasm.

● Slide: part of slide pink, other area darker. Large, light pink area = necrosis. Many
new, small granuloma around large area of necrosis. Epithelioid cells (elongated
nucleus). Can be layers of necrosis mixed with layers of fibrosis
 Sarcoidosis of the lung (313)

● Worldwide disease affecting all races and sexes

● Causes are multifactorial – environmental and genetic (BTNL gene)
● lung, lymph nodes, spleen, liver, skin, uveal tract, bone marrow
● Granulomatous inflammation
● No caseous necrosis
● multiple, sarcoid granulomas are scattered in the interstitium of the lung
● granuloma – lymphocytes, giant cells, epithelioid cells (macrophages)
● Asteroid bodies (star shaped crystals) may be seen
● Schaumann bodies (small calcifications with a laminar structure) may be present
inside Langhans cells.
● slide: lymphocytes on the edges, central part with epithelioid cells (not just on the
edge like regular granuloma). Giant cells. Many granulomas.
 Silicosis of the lung (323)

Whorl of collagen

● Caused by the inhalation of silicon dioxide

○ Silica particles are ingested by alveolar macrophages
○ Macrophages are destroyed by silica particles
○ dead cells release free silica particles and fibrogenic factors
○ fibrogenic factors form nodules of collagen fibers.
● Usually slowly progressing, nodular, fibrosing pneumoconiosis.
● Silicotic nodule is composed of concentric whorls of dense, sparsely cellular collagen
● Infiltration composed of lymphocytes and macrophages
● At the edge of the nodule – dust with carbon pigment and silica particles
○ silica particles are hard to see
● Slide: nodule surrounded by chronic inflammatory cells (Coal dusts, macrophages,
lymphocytes). Few cells in nodule (collagen fibers).